AI Article Synopsis
- The type II voltage-dependent sodium channel gene is only expressed in neurons due to a silencer element that functions in nonneuronal cells.
- A transcription factor known as REST binds to this silencer, preventing the gene from being active outside of neurons.
- In developing mouse embryos, REST is present everywhere but is active in nonneuronal cells to block the expression of the sodium channel gene, suggesting that neural expression occurs by default when REST is absent.
Article Abstract
Expression of the type II voltage-dependent sodium channel gene is restricted to neurons by a silencer element active in nonneuronal cells. We have cloned cDNA coding for a transcription factor (REST) that binds to this silencer element. Expression of a recombinant REST protein confers the ability to silence type II reporter genes in neuronal cell types lacking the native REST protein, whereas expression of a dominant negative form of REST in nonneuronal cells relieves silencing mediated by the native protein. REST transcripts in developing mouse embryos are detected ubiquitously outside of the nervous system. We propose that expression of the type II sodium channel gene in neurons reflects a default pathway that is blocked in nonneuronal cells by the presence of REST.
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| http://dx.doi.org/10.1016/0092-8674(95)90298-8 | DOI Listing |
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